ELABELA: A hormone essential for heart development signals via the apelin receptor

Serene C. Chng; Lena Ho; Jing Tian; Bruno Reversade

doi:10.1016/j.devcel.2013.11.002

ELABELA: A hormone essential for heart development signals via the apelin receptor

Serene C. Chng, Lena Ho, Jing Tian, Bruno Reversade

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382 Scopus citations

Abstract

We report here the discovery and characterization ofa gene, ELABELA (ELA), encoding a conserved hormone of 32 amino acids. Present in human embryonic stem cells, ELA is expressed at the onset of zebrafish zygotic transcription and is ubiquitous in the naive ectodermal cells of the embryo. Using zinc-finger-nuclease-mediated gene inactivation in zebrafish, we created an allelic series of ela mutants. ela null embryos have impaired endoderm differentiation potential marked by reduced gata5 and sox17 expression. Loss of Ela causes embryos to develop with a rudimentary heart or no heart at all, surprisingly phenocopying the loss of the apelin receptor (aplnr), which we show serves as Ela's cognate G protein-coupled receptor. Our results reveal the existence of apeptide hormone, ELA, which, together with APLNR, forms an essential signaling axis for early cardiovascular development. © 2013 Elsevier Inc.

Original language	English (US)
Pages (from-to)	672-680
Number of pages	9
Journal	Developmental Cell
Volume	27
Issue number	6
DOIs	https://doi.org/10.1016/j.devcel.2013.11.002
State	Published - Dec 23 2013
Externally published	Yes

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Generated from Scopus record by KAUST IRTS on 2023-02-15

ASJC Scopus subject areas

Developmental Biology

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10.1016/j.devcel.2013.11.002

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title = "ELABELA: A hormone essential for heart development signals via the apelin receptor",

abstract = "We report here the discovery and characterization ofa gene, ELABELA (ELA), encoding a conserved hormone of 32 amino acids. Present in human embryonic stem cells, ELA is expressed at the onset of zebrafish zygotic transcription and is ubiquitous in the naive ectodermal cells of the embryo. Using zinc-finger-nuclease-mediated gene inactivation in zebrafish, we created an allelic series of ela mutants. ela null embryos have impaired endoderm differentiation potential marked by reduced gata5 and sox17 expression. Loss of Ela causes embryos to develop with a rudimentary heart or no heart at all, surprisingly phenocopying the loss of the apelin receptor (aplnr), which we show serves as Ela's cognate G protein-coupled receptor. Our results reveal the existence of apeptide hormone, ELA, which, together with APLNR, forms an essential signaling axis for early cardiovascular development. {\textcopyright} 2013 Elsevier Inc.",

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AU - Chng, Serene C.

AU - Ho, Lena

AU - Tian, Jing

AU - Reversade, Bruno

N1 - Generated from Scopus record by KAUST IRTS on 2023-02-15

PY - 2013/12/23

Y1 - 2013/12/23

N2 - We report here the discovery and characterization ofa gene, ELABELA (ELA), encoding a conserved hormone of 32 amino acids. Present in human embryonic stem cells, ELA is expressed at the onset of zebrafish zygotic transcription and is ubiquitous in the naive ectodermal cells of the embryo. Using zinc-finger-nuclease-mediated gene inactivation in zebrafish, we created an allelic series of ela mutants. ela null embryos have impaired endoderm differentiation potential marked by reduced gata5 and sox17 expression. Loss of Ela causes embryos to develop with a rudimentary heart or no heart at all, surprisingly phenocopying the loss of the apelin receptor (aplnr), which we show serves as Ela's cognate G protein-coupled receptor. Our results reveal the existence of apeptide hormone, ELA, which, together with APLNR, forms an essential signaling axis for early cardiovascular development. © 2013 Elsevier Inc.

AB - We report here the discovery and characterization ofa gene, ELABELA (ELA), encoding a conserved hormone of 32 amino acids. Present in human embryonic stem cells, ELA is expressed at the onset of zebrafish zygotic transcription and is ubiquitous in the naive ectodermal cells of the embryo. Using zinc-finger-nuclease-mediated gene inactivation in zebrafish, we created an allelic series of ela mutants. ela null embryos have impaired endoderm differentiation potential marked by reduced gata5 and sox17 expression. Loss of Ela causes embryos to develop with a rudimentary heart or no heart at all, surprisingly phenocopying the loss of the apelin receptor (aplnr), which we show serves as Ela's cognate G protein-coupled receptor. Our results reveal the existence of apeptide hormone, ELA, which, together with APLNR, forms an essential signaling axis for early cardiovascular development. © 2013 Elsevier Inc.

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JO - Developmental Cell

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ELABELA: A hormone essential for heart development signals via the apelin receptor

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